1. Field of the Invention
This invention relates generally to a dietary supplement for decreasing or eliminating pain and particularly relates to a composition which promotes the transport of tryptophan from the blood into the brain.
2. Description of Prior Developments
Attention has recently turned to nontraditional methods and compositions for reducing pain in an effort to provide relief in those instances where standard techniques have proven ineffective and where it is desired to avoid the well-known drawbacks of conventional analgesics. One approach has been to attempt to relieve pain through dietary supplementation of L-tryptophan (tryptophan). Once within the brain, neurons convert tryptophan into the neurotransmitter serotonin. It has been found that an increase of tryptophan in the brain increases the brain production of serotonin which has been shown to be linked to sleep, appetite, depression, and pain threshold. Disturbances in the brain causing reduced levels of serotonin have been linked to clinical depression, insomnia, and lowered pain threshold. The latter abnormality results in chronic intractable pain.
It is known that dietary supplementation of tryptophan increases the blood level of tryptophan and facilitates the passage of tryptophan across the blood-barrier into the brain. The increased amount of tryptophan in the brain permits a greater amount of tryptophan to be converted to the compound, serotonin.
The level of one's pain threshold, a mechanism that normally prevents the brain from interpreting stimuli below a certain level as pain, is directly related to the amount of serotonin that is present in the brain. The higher the level of serotonin that is present, the higher will be the pain threshold level, up to a normal maximum level. With normal amounts of serotonin one can function in a normal manner and not be subjected to myriad numbers of stimuli such as from muscle activity, that could manifest themselves as pain impulses.
In order for tryptophan to be converted to serotonin in the brain, it must cross a separating mechanism that exists between the blood vessel and the brain. To reach the brain, tryptophan requires a carrier transport mechanism which, literally, carries tryptophan across this very selective blood-brain barrier and into the brain. Because of its polar nature, tryptophan requires a carrier protein to transport it across the blood-brain barrier. Not only is tryptophan carried by this transport mechanism, but other selected amino acids, called large neutral amino acids, (LNAAs) are carried as well. Tryptophan not only has to compete with these LNAAs for access to the transport carrier mechanism, it also has a lower affinity for the carrier system than does the LNAAs. To compound this situation further, tryptophan in foods is generally present in lower amounts than the LNAAs - particularly in animal proteins. All of these factors contribute to the amount of tryptophan that actually gets through to the brain, to be finally converted into serotonin.
There are numerous conditions, improper diet constitutes one of them, that can interfere with, and decrease, the amount of tryptophan that normally passes through the blood-brain barrier into the brain each day. This comes about when the ratio of tryptophan to LNAAs in the blood going to the brain is lower than normal. This means that the number of molecules of tryptophan present at the blood-brain barrier is much smaller than the number of LNAAs present at the same blood-brain barrier. The LNAAs overwhelm the tryptophan and very little tryptophan is provided passage into the brain, compared to the number of LNAAs that are provided passage.
In the attempt to correct this improper tryptophan/LNAA ratio, it was found that increasing the total protein intake, obtained from normal dietary sources, in order to add more tryptophan to the system, results, paradoxically, in an even greater decrease in the pain threshold level. This is so because there are usually more LNAAs than there is tryptophan in food. Experimental studies have established the fact that increasing the amount of protein as food, in order to improve the tryptophan/LNAA ratio, only makes the tryptophan/LNAA ratio worse because of the greater intake of the LNAAs over the intake of the tryptophan.
With less tryptophan getting into the brain, less serotonin is formed, and the pain threshold is lowered. Whereas, under normal conditions, low-level sensory perceptions interpreted by the body as pain stimuli would have been filtered out by the normal pain threshold level, they are now experienced as pain. This pain can span the gamut from relatively insignificant annoyances to chronic, unremitting, intractable, excrutiating pain. Because this type of pain stems from a biochemical imbalance involving the tryptophan-serotonin relationship which cannot be corrected by any medication, it is unmanageable by any conventional drug therapy - because the drug does not address itself to the correction of this specific biochemical imbalance.
Accordingly, a need exists for a method and composition for transporting an effective dose of tryptophan across the blood-brain barrier into the brain and for promoting the conversion of tryptophan into serotonin.